T(H)17 cells mediate pulmonary collateral priming.

Background: Our laboratory has shown that inhalational sensitization to new antigens is facilitated through an ongoing T(H)2-polarized inflammation of the lung, a phenomenon we call "collateral priming."

Objective: We were interested to analyze whether a T(H)1-polarized pulmonary inflammation also facilitates priming toward new antigens and which cytokine or cytokines are involved.

Methods: T(H)1-polarized T cells were generated in vitro and transferred into congenic mice.

TLR4 signaling in stromal cells is critical for the initiation of allergic Th2 responses to inhaled antigen.

Allergic asthma is an inflammatory lung disease driven by Th2. We have shown that both Th1 and Th2 sensitization to inhaled OVA depend on the presence and concentration of LPS, where high concentrations (LPS(hi)) induce Th1 and low concentrations (LPS(lo)), Th2. Stromal cells (SCs), such as airway SCs, exacerbate established airway disease; however, little is known about their role early during sensitization.

A new mechanism for inhalational priming: IL-4 bypasses innate immune signals.

Signaling via innate immune mechanisms is considered pivotal for T cell-mediated responses to inhaled Ags. Furthermore, Th2 cells specific for one inhaled Ag can facilitate priming of naive T cells to unrelated new inhaled Ags, a process we call "Th2 collateral priming". Interestingly, our previous studies showed that collateral priming is independent of signals via the innate immune system but depends on IL-4 secretion by CD4(+) T cells.

3H-uridine incorporation by small lymphocytes of tolerant rats: relationship to T and B lymphocytes.

Tissue tolerance was induced in neonatal rats by the intravenous injection of bone marrow cells from adult allogeneic rat donors. After 6 to 8 weeks, lymphoid cells from rats in which tolerance had been induced were tested for mixed lymphocyte reactivity (MLR), 3H-uridine uptake, and the relationship of uridine incorporation to B and T lymphocytes. Lymph node (LN) and spleen (SPL) cells from the adult inoculated rats showed no reactivity in the MLR or normal lymphocyte transfer reaction (NLTRx), indicating that the animals were tolerant.